Field of the Invention
The invention relates generally to a method for mitigating methylenetetrahydrofolate reductase (MTHFR) associated polymorphisms and specifically to stable formulations of the active form of folic acid, 5-methyltetrahydrofolate (MTHF).
Background Information
This invention relates to a method for mitigating methylenetetrahydrofolate reductase (“MTHFR”) associated polymorphisms. MTHFR is an enzyme responsible for converting 5,10-methylenetetrahydrofolate to the active end product of folic acid, 5-methyltetrahydrofolate. Particularly, this invention relates to addressing MTHFR deficiency and its relation to chronic degenerative disease. Delivery of 5-methyltetrahydrofolate (MTHF), via a more direct route of delivery than is currently available is addressed.
Folic acid is commonly found in green leafy vegetables, legumes, nuts, orange juice and some fruits. Folic acid is a water-soluble form of vitamin B9 that the body requires for cell growth and reproduction.
When digesting folic acid the body goes through several steps in order to “break down” the folic acid to its active form, 5-methyltetrahydrofolate, so it can be used properly. This is a complex process which is shown, step-by-step, in FIG. 1. As a result of these steps, the body makes a version of folic acid called MTHF.
Methyl groups are utilized extensively in the body for transport of nutrients in fat soluble states and in epigenetic processes, turning genes on or off. In patients with decreased activity in the methylation pathway, there is a shortage of methyl groups in the body required to execute a variety of important functions. Additionally, defects in methylation lay the appropriate groundwork for the further assault of environmental and infectious agents resulting in a wide range of conditions including diabetes, cardiovascular disease, thyroid dysfunction, neurological inflammation, diabetes, chronic viral infection, neurotransmitter imbalances, atherosclerosis, cancer, aging, schizophrenia, decreased repair of tissue damage, improper immune function, neural tube defects, Down's syndrome, Multiple Sclerosis, ADHD, Huntington's disease, Parkinson's disease, Alzheimer's and autism. Appropriate supplementation with vitamins and nutrients bypasses these mutations to allow for restored function of the pathway.
Not every individual with mutations in the methylation pathway will have one of the health conditions listed above. While may be a necessary element, there may not be a sufficient environmental or infectious trigger. Most health conditions in society today are multifactorial in nature. In essence, there is an underlying genetically determined risk that requires a significant infectious or environmental trigger to initiate the process. A certain threshold or body burden needs to be met for each of these factors in order for multifactorial disease to occur. However, part of what makes the methylation cycle so unique and so critical for health, is that mutations in this pathway have the capability to impair all three of these factors. This suggests that if an individual has sufficient mutations or weaknesses in their methylation pathway, this may be sufficient to cause the multifactorial disease by itself, as methylation cycle mutations can lead to chronic infectious diseases, increased environmental toxin burdens and have secondary effects on genetic expression.
According to a national testing laboratory, it is estimated that up to 45% of the United States population may have a mutation in at least one gene. Additionally, it has been reported that 70% of an identified depressed population has a MTHFR mutation. Conventional treatment for MTHF deficiency includes oral intervention with the vitamins folic acid and cyanocobalamin, which are inactive forms of these entities. The body must then convert both folic acid and cyanocobalamin to the active forms before it is able to utilize them. If one has a methylation mutation, they lack the ability to achieve this critical conversion. Studies illustrate that if an individual has compromised gut health, absorption of these vitamins may be greatly reduced. Therefore, there is a demand for a new stable route of delivery and new stable formulations that circumvent potential problems associated with oral absorption and/or inability to convert due to mutation.